First Aid: Respiratory Flashcards
In which cases does FRC increase?
Advanced Age and Asthma Attack
Shifting the O2 dissociation curve to the right will _________ unloading of O2 in the tissue?
Increase
What increases unloading of O2 in the tissues (i.e. shifts O2 dissociation curve to the right)?
Increases in BAT ACE
BPG, Altitude, Temperature, Acid, CO2, Exercise
What are the normal concentrations of pH, PCO2, and bicarbonate in arterial blood?
pH: 7.35-7.45
PCO2: 40 mmHg
bicarbonate: 22-28 mmol/L
Where are the relative levels of ventilation and perfusion in the apex and base of the lung?
BOTH V and Q are increased at the base of the lung. But V/Q is higher at the apex.
A patient presents with increased sinus congestion and complains of tenderness in the region of his maxillary sinuses. What is his disease and what are the top 4 common causes of it?
Rhinosinusitis
- Viral upper respiratory tract infection
- S. Pneumoniae
- H. influenzae
- M. catarrhalis
A 50 y/o woman recently arrived from a long flight from Australia. She is currently battling breast cancer and has a history of smoking and high cholesterol. She complains of calf pain on dorsiflexion of the foot. What would you opt to treat her with in an acute and long term setting? (also describe the 3 major risk factors for her disease)
May have Deep Vein Thrombosis (Virchow’s Triad: 1. Stasis, 2. Hypercoagulability -commonly factor V Leiden- 3. Endothelial damage)
Tx: Heparin for acute management, Warfarin for long term DVT management
What are the common causes of a shunt, and how can you detect its presence?
AV malformation or consolidated pneumonic lobule.
Give pure O2 to breath and notice how PAO2 will not increase as much as it should.
Patient presents with cyanosis and chocolate-colored blood. What does he have and what would you treat him with? What do you NOT want to give the patient?
Methemoglobinemia (oxidized form of Hb, w/ decreased affinity for O2 and increased affinity for cyanide)
Give Methylene blue. DO NOT give Nitrites.
How can you treat cyanide Poisoning?
Give nitrite to oxidize Hb to methemoglobin (which binds cyanide). Thiosulfate to bind this cyanide –> Thiocyanate –> Renal excretion
What is the normal level of Hb in your blood, and when would you develop cyanosis?
Normal: 15 g/dL
Cyanosis: deoxygenated Hb > 5 g/dL
A 58 year old man with a 40 pack year history presents with shortness of breath (increasing over past few years). He has some cough with little sputum and marked chest overexpansion. He is non-cyanotic with quiet breath sounds, hyperresonance on percussion, and he seems to be breathing through pursed lips. He is experiencing some weight loss as well. What would you expect to see on a gross specimen of his lungs, as well as on histological slides? What would happen to his FRC?
Pink Puffer - barrel shaped chest - emphysema - INCREASED FRC
Centracinar emphysema, multiple air space cavities lined by heavy black carbon deposits on gross specimen.
On microscopy, enlarged alveoli separated by thin septa.
Why does the chest wall expand with emphysema?
Increased elastase activity, loss of elastic fibers and increased lung compliance.
Lung isn’t able to push in as readily and expands into chest wall (loses lung/chest wall tug of war).
A 32 year-old nonsmoker presents with shortness of breath and mild to very little cough (no sputum). He complains of loss of appetite, fatigue, and a brownish orange tint on his urine. He is jaundiced and shows signs of edema in legs and ankles. A liver biopsy is taken; what do you see? What genetic mutation may he have?
On biopsy you see round dark purple/pink (PAS+) globules in the hepatocytes (this is alpha-1 antitrypsin accumulation).
A1AT Deficiency - panacinar emphysema may also be present.
A 54 year old man with a 30 pack year history presents with SOB and frequent productive cough over the past 4 months. This has been occuring for some years now. He is cyanotic and you hear wheezing and rales on auscultation. You also notice some peripheral edema. What would you expect his Reid index to be on biopsy of bronchiole tissue? What would you possibly see on echocardiography?
> 50%, from hyperplasia of mucus-secreting glands in bronchi
Right Ventricular Hypertrophy as a result of right heart failure. Cor pulmonale, because arterioles clamp down everywhere to shunt blood to well perfused regions. Now heart has to pump against increased pulmonary tension.
A 45 year old woman presents to the ER with shortness of breath and chest pain. She seems disoriented and confused and has signs of petechial rash. An ABG shows low oxygen levels. Her husband who is with her states that she has no major prior medical history, other than a recent liposuction that she received by a plastic surgeon from a local clinic. She was resting in bed for many days following surgery. What test should you do immediately? You see the tests results, what is she suffering from and what are other major causes for this?
CT pulmonary angiography to look for filling defects as a result of Pulmonary Embolism from a fat embolus
Causes include FAT BAT:
-Fat (following liposuction and long bone fractures)
-Air (nitrogen bubbles in ascending divers -need hyperbaric oxygen)
-Thrombus (DVT)
-Bacteria
-Amniotic fluid (can lead to disseminated intravascular coagulation, especially post-partum)
Tumor (hypercoagulability)
What is the MOA of beta 2 agonists?
Increased adenalyl cyclase activity in the smooth muscles, increasing intracellular cAMP, decreasing muscle contraction
What three conditions are associated with Type I allergic hypersensitivity reaction of asthma?
- Allergic Rhinitis
- Eczema
- Family History of Atopy
What are three non-allergenic causes of asthma?
- Exercise
- Viral URI
- Aspirin intolerant asthma
A 2 year old is brought in because of difficulty breathing. The parents state that the child has had multiple bouts of a “cold” over the past year and now frequently breathes out of her mouth. Rhinoscopy reveals nasal polyps. What do you immediately want to screen the child for?
Cystic fibrosis
A 27 year old man who works on Wall Street presents to the ER with wheezing and SOB. He wasn’t feeling well in the morning following a night of heavy drinking and decided to take something for his headaches. He was at a female friends house and took “something she had laying around”. What drug did he take, and what would you find on physical exam?
He took aspirin triggering an asthmatic exacerbation as a result of aspirin intolerant asthma.
On PE or rhinoscopy you may find nasal polyps.
What are the key histopathological findings in someone with asthma, and how did these arise?
- Smooth muscle hypertrophy
- Curschmann spirals (shed epithelium forms mucous plugs)
- Charcot-Leyden Crystals (from breakdown of eosinophils in sputum)
What are the key clinical symptoms in someone with asthma?
Wheezing, cough, tachypnea, dyspnea, hypoxemia, decreased I/E ratio, pulsus paradoxus, mucus plugging
A 63 year old smoker presents with difficulty on expiration. He is a severe cough, SOB, and produces a purulent sputum, with occasional traces of blood. Laboratory tests reveal a decreased PAO2. What does this patient have, how did it develop, and why is it so difficult to expire?
Bronchiectasis
Damage to the walls of the airway (especially the cilia) as a result of chronic necrotizing infection of the bronchi. Smoking caused it in this case.
Resulting dilation of bronchi results in loss of tone and air trapping. Dilation of airways does not allow for the air to accelerate out.
What are the 5 main associations with bronchiectasis and the pathological processes that lead to this disorder?
Necrotizing Inflammation: In all cases the pathophysiology is a result of necrotizing inflammation following infections.
- Smoking: reduced ciliary motility
- Cystic fibrosis: big secretions and mucous plugging lead to increased infection
- Kartagener Syndrome: Defective dynein arm of cilia (also have sinusitis, infertility and organ inversus)
- Tumor or foreign body: airway block –> infection
- Allergic bronchopulmonary aspergillosis: hypersensitivity reaction to aspergillus bug leading to inflammation of airway
An allergen activates the TH2 phenotype of CD4+ T cells in genetically susceptible individuals resulting in the secretion of certain factors. What are these factors and what do they in turn activate?
Pathophysio process of Asthma:
IL4 -> IgE activation
IL5 -> Eosinophils activated
IL10 -> increases TH2 and inhibits TH1 perpetuation disease
Re-exposure to an allergen that activated TH2 phenotype and led to immune response will cause what cascade of events, leading to early phase asthma exacerbation?
Early Phase: Crosslinking of MAST cells –> Histamine release –> 1) vasodilation, leaky capillaries 2) Leukotrienes C4, E4 -bronchoconstriction via sm. muscle contraction - D4 - increased vascular permeability- and overall vasoconstriction 3) increased vascular permeability
What compound perpetuates late phase bronchoconstriction in asthma?
Major Basic Protein